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• W4387248766 abstract "SESSION TITLE: Critical Care Case Report Posters 39 SESSION TYPE: Case Report Posters PRESENTED ON: 10/10/2023 09:40 am - 10:25 am INTRODUCTION: Cerebral Amyloid Angiopathy (CAA), a small vessel cerebral angiopathy caused by β-amyloid deposition, is a common etiology for spontaneous intracerebral hemorrhage (ICH) in patients admitted to the ICU, specifically older adults presenting with lobar bleeds. Management of these patients is symptomatic, and prognosis usually depends on the size of the bleed and comorbidities [1]. However, there is a subtype of CAA, Cerebral Amyloid Angiopathy-Related Inflammation (CAA-RI), that can present acutely with aggressive symptoms such as seizures and rapidly progressive dementia [2]. Here we present the case of a patient who developed severe diffuse cerebral edema and elevated intracranial pressure due to CAA-RI. CASE PRESENTATION: A 69-year-old African American female with dementia and prior occipital hemorrhagic stroke, presented to the emergency department after being found unresponsive in her bathroom. On arrival, she was lethargic with leftward gaze deviation and making grunting noises. Her pupils were equal and reactive, and she was moving all four extremities spontaneously. Initial CT head demonstrated bilateral sulci effacement with multiple foci of acute intraparenchymal hemorrhage involving the left parietal and temporal lobes and evolving right occipital lobe hematoma. Imaging revealed no evidence of skull fractures, contusions, venous sinuses thrombosis, large vessel occlusion, aneurysm, masses, or venous malformations. She was intubated and transferred to the ICU. An intraparenchymal pressure monitor (bolt) was placed and intracranial pressure (ICP) was noted to be 22cmH20. Propofol was initiated but her ICP increased to 50cmH20 in a matter of hours, and she was no longer moving her upper extremities spontaneously. A bolus of 23.4% NaCl was delivered along with mannitol 0.5mg/kg with initial improvement in ICP. Hypertonic saline was continued at 30cc/hour and propofol was increased to maximum dose. However, her ICP continued to rise, peaking at 70cmH20. Phenobarbital and midazolam were added, and she was paralyzed with cisatracurium. The bolt monitor was exchanged for an external ventricular drain (EVD) set at 0cmH20. Repeat CT head demonstrated worsening cerebral edema with diffuse sulcal effacement. Over the next 24 hours her ICP improved and remained less than 5cmH20. An MRI brain with and without contrast was performed that demonstrated confluent hyperintensities on T2 fluid-attenuated inversion recovery sequence with multifocal intracranial hemorrhage including innumerable prominent lobar microhemorrhages suggestive of cerebral amyloid angiopathy-related inflammation. She was started on high dose IV solumedrol for five days with continued improvement in cerebral edema and her EVD was removed. Her hospital course was complicated by recurrent seizures, pneumonia, and chronic hypoxemic respiratory failure requiring tracheostomy. She was eventually discharged to a long-term acute care facility in stable condition. DISCUSSION: The gold standard for diagnosing CAA-RI is biopsy, however this is invasive, and a probable diagnosis can be made based on clinical presentation and imaging [2,3]. Studies show that immunosuppressive therapy improves the initial disease course and reduces the likelihood of recurrence [3]. CONCLUSIONS: Patients presenting to the ICU with spontaneous ICH may have underlying CAA, however it is important to recognize the rare subtype, CAA-RI, in patients presenting atypically, as early recognition and disease specific management can be lifesaving. REFERENCE #1: de Oliveira Manoel, A.L., Goffi, A., Zampieri, F.G. et al. The critical care management of spontaneous intracranial hemorrhage: a contemporary review. Crit Care 20, 272 (2016). https://doi.org/10.1186/s13054-016-1432-0 REFERENCE #2: Grasso D, Castorani G, Borreggine C, Simeone A, De Blasi R. Cerebral amyloid angiopathy related inflammation: A little known but not to be underestimated disease. Radiol Case Rep. 2021;16(9):2514-2521. Published 2021 Jul 3. doi:10.1016/j.radcr.2021.05.080 REFERENCE #3: Regenhardt RW, Thon JM, Das AS, et al. Association Between Immunosuppressive Treatment and Outcomes of Cerebral Amyloid Angiopathy-Related Inflammation. JAMA Neurol. 2020;77(10):1261-1269. doi:10.1001/jamaneurol.2020.1782 DISCLOSURES: No relevant relationships by Audrey Demand No relevant relationships by Muhammad Malik" @default.
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• W4387248766 date "2023-10-01" @default.
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• W4387248766 title "THE PRESSING ISSUE: A CASE OF NONTRAUMATIC ELEVATED INTRACRANIAL PRESSURE DUE TO CEREBRAL AMYLOID ANGIOPATHY-RELATED INFLAMMATION (CAA-RI)" @default.
• W4387248766 doi "https://doi.org/10.1016/j.chest.2023.07.1423" @default.
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